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. 2018 Jul 25;8:11198. doi: 10.1038/s41598-018-29558-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed model of the relation between haemolysis, IL-10, HO-1 and mortality at admission of sepsis. The majority of sepsis patients at admission are moderately anaemic (low haemoglobin); however, those with the highest erythrocyte counts show elevated markers of haemolysis (haem and haemopexin, HPX) and elevated EPO. Further, systemic infection leads to robust inflammation and correlated with haemolysis (depleted haemopexin levels). Next, we observed that both IL-10 and haemolysis (depleted haemopexin) leads to the induction of haem-oxygenase 1 (HO-1). After partial correlation analysis for HO-1 induction which adjusted for either factor (IL-10 or haem and HPX), we found that IL-10 was the main driver of HO-1. IL-10 and HO-1 both individually showed a significant and moderate correlations to clinical severity score (APACE II, SOFA). Finally, high levels of IL-10, HO-1, and haem (i.e., above median value) at admission were positively associated with in-hospital mortality. Of note, this proposed model is limited to the ICU admission parameters measured in this study – long-term interaction pathways and their full consequences is currently unclear. The causal model (i.e., the direction of the arrows) was determined a priori and tested using the study data, Arrow size: 1 pt (p = 0.05–0.02), 3 pt (p = 0.019–0.001), and 6 pt (p < 0.001).